Three different levels of global forebrain ischemia were induced in rats and their plasma levels of Thromboxane B2 (TXB2) and 6 Keto PGF1.alpha. were determined to investigate the relation between severity of ischemia and eicosanoid production. Ischemia stimulates the activity of cellular lipase whose actions cause deacylation of brain phospholipids and release of free fatty acids. Arachidonic acid (A.A.) is one of the predominant fatty acids which is liberated in brain after ischemia. A.A. in the primary substrate for the synthesis of prostaglandins (PGs). Thromboxane A2 (TXA2) and Prostacyclin (PGI2), which play an important role in regulation of platelet aggregation and vasotonus. Thromboxane is a potent platelet aggregator and vasoconstrictor. On the other hand, PGI2 has the opposite nature. Therefore it can be considered that PGs and moreover, the balance of TXA2 and PGI2 may have an intimate relation to the development of cerebral ischemia. Three different levels of ischemia were produced by bilateral carotid artery ligation (BLCL) using three kinds of rats with different blood pressure ranges, namely, SHRSP (Stroke-prone spontaneously hypertensive rats), SHRSR (Stroke-resistant spontaneously hypertensive rats) and WKY (Wistar Kyoto rats). It is known that higher pressure groups suffer severe ischemia by BLCL procedure. Hypertensive rats (SHRSP, SHRSR) were originally produced from WKY. The experimental animals used were about 300 gr and 16 weeks old male rats. The plasma and brain TXB2 and 6 Keto-PGF1.alpha., stable metabolites of TXA2 and PGI2 were measured by radioimmunoassay. The chronological changes of brain and plasma PGs levels after ischemia using SHRSR were also investigated. Colloidal carbon perfusion was performed on rats 3hr. after BLCL. CBF and brain water content were measured and compared to the PGs levels. In the hypertensive groups (SHRSP and SHRSR), colloidal carbon perfusion showed a markedly disturbed pattern, whereas the carbon was well filled in normotensive WKY. The hypertensive rats (SHRSP, SHRSR) demonstrated severe decrease of CBF with increase of brain edema 3hr. after BLCL. While the normotensive rats showed only slight decrease of CBF and did not have increase of water content. Plasma TXB2 3hr. after BLCL showed a significant increase in the hypertensive groups but no change was observed in normotensive WKY. On the other hand, 6 Keto PGF1.alpha. showed a similar increase in these three groups of rats. On the periodical observation using SHRSR, plasma TXB2 continuously increased after BLCL and was significantly increased after 3hr. of BLCL. 6 Keto PGF1.alpha. showed a continuous increase but the increase was slight compared to that of TXB2. The cerebral tissue TXB2 and 6 Keto PGF1.alpha. also showed a remarkable increase at 3hr. after BLCL but the increase was more prominent in TXB2. The increase of TXA2 and the priority of TXA2 over PGI2 were demonstrated in the plasma and tissue to the hypertensive groups of rats which suffered a more severe ischemic damage by BLCL. It may play an important role in developing ischemia due to the biological activities of TXA2.